Received March 2, 2004
Revised March 30, 2004
Accepted after revision April 27, 2004

¹ Howard Florey Institute

^* To whom correspondence should be addressed. E-mail: r.woods{at}hfi.unimelb.edu.au.

	Abstract

Atrial natriuretic peptide (ANP) enhances cardiac vagal baroreflexes in normotensive animals. In spontaneously hypertensive rats (SHR) this effect of ANP was absent. ANP's reflex actions were preserved if hypertrophy was completely prevented in SHR. However even a small amount of cardiac hypertrophy, with no hypertension, in SHR was accompanied by a loss of the reflex bradycardic actions of ANP. In the present study, we investigated whether pathophysiological cardiac hypertrophy, induced by one-kidney, one-clip renovascular hypertension (1K-1C; n=6), or physiological cardiac hypertrophy induced by chronic spontaneous, wheel-running exercise training (n=7), similarly prevented vagal reflex actions of ANP. Cardiac baroreceptor-activated bradycardia was measured during rapid ramp increases (5sec) in blood pressure after bolus methoxamine doses in conscious, chronically instrumented rats during infusions of ANP (50 pmol kg^-1 min^-1) or vehicle. Compared with uninephrectomized control rats (n=10), 1K-1C had cardiac hypertrophy (55% increase in left ventricle:body weight ratio (LV:BW); P<0.05) and blunted vagal baroreflex gain (-0.93±0.18 vs -0.50±0.13 bpm mmHg^-1; P<0.05). ANP did not improve baroreflex function in 1K-1C. Compared with their sedentary controls (n=7), exercise-trained rats with cardiac hypertrophy (20% increase LV:BW; P<0.05) also had blunted ramp baroreflex bradycardia (-1.28±0.23 vs -0.57±0.09 bpm mmHg^-1; P<0.05). By contrast, ANP more than doubled baroreflex bradycardia in exercise-trained rats (P<0.05). The etiology of cardiac hypertrophy, therefore, influenced whether ANP retains its vagal baroreflex enhancing properties.

Key Words: Cardiovascular, Hypertension, Natriuretic peptide